OBJECTIVE: Alzheimer's disease (AD) stands as the prevalent neurodegenerative condition globally, characterized by symptoms such as memory loss, language difficulties, disorientation, diminished motivation, self-neglect, mood fluctuations, and behavioral challenges. Despite its widespread impact, the precise cellular mechanisms underlying the onset of AD remain elusive. This study aims to uncover potential pathophysiological contributors to AD by analyzing gene expression levels through bioinformatics approaches. METHODS: GSE129296 dataset downloaded from Gene Expression Omnibus (GEO) database was re-examined for this research. In the dataset, pre-pathologic (n=4) and pathologic (n=4) microglia were isolated from cortical and hippocampal regions of TAU mice at 3 and 9-month-old. After gene expression levels in the dataset were re-analysed in R program, based on Benjamini-Hochberg correction, adjusted p-values <0.05 were accepted as significant. Gene set enrichment analyses were performed in Gene Ontology (GO) and ENRICHR tools. RESULTS: Gene expression levels indicated that pro-opiomelanocortin (POMC), galectin (LGALS-1,3,9,3BP), diazepam binding inhibitor (DBI), periostin (POSTN), ubiquitin like-5 (UBL5), retinoic acid receptor responder-2 (RARRES2), nerve growth factor receptor associated protein-1 (NGFRAP1), some chemokine (CCL3-5, CXCL10) genes were upregulated (p<0.05); and arginine vasopressin receptor-2 (AVPR2), islet amyloid polypeptide (IAPP), endothelin-1 receptor (EDNR1), vasoactive intestinal peptide receptor-1 (VIPR1), period circadian regulator-1 (PER1) genes were downregulated (p<0.05) in pathologic AD group, compared with pre-pathologic AD group. CONCLUSION: Results from this study indicate imbalances in the expression levels (up- and down-regulation) of genes known to be involved in many neuroendocrine signaling in microglial cells during the developmental process of AD.